1. Technical Field
The invention belongs to the field of medicine and particularly relates to the application of irisin in the preparation of drugs for preventing myocardial ischemia reperfusion injuries.
2. Description of Related Art
Ischemic heart disease is one of the main diseases leading mortality in the world and greatly threatens human health. The pathology of ischemic cardiomyopathy is shown as that due to blood vessel blockages caused by coronary atherosclerosis or thrombosis, blood circulation is suffocated or interrupted which unbalances the myocardial oxygen and energy supply and disrupts the myocardial energy metabolism, and histopathological damage is caused, such as myocardial infarctions and heart failure. At present, the most effective treatment method for overcoming ischemia is blood vessel re-dredging for blood supply restoration, including balloon dilatation, arteriovenous thrombolysis, extracorporeal circulation, coronary artery bypass surgery and the like, namely reperfusion. However, after myocardial ischemia reperfusion injuries were put forward in 1960 for the first time, medical workers have been plagued by this problem, a large number of animal experiments and clinical results show that although reperfusion greatly improves the myocardial blood supply, instead further worsening of the tissue damage caused during ischemia is seen due to the fact that a large amount of oxygen-rich blood and other nutrients flows into the ischemic area, and arrhythmia, cardiac rupture, heart failure and other complications are caused. Clinical studies show that myocardial ischemia reperfusion injuries are very common in cardiovascular surgery and account for a large proportion of early death caused by coronary artery bypass surgery, myocardial infarction, heart transplantation failure and so on and so forth. Therefore, how to prevent and abate myocardial reperfusion injuries has become a significant clinical topic.
The specific mechanism of myocardial ischemia reperfusion injuries remains unclear. Myocardial ischemia causes insufficient energy metabolism and ATP depletion, intracellular calcium overload occurs in the reperfusion process producing a large number of oxygen free radicals, and membrane phospholipids, proteins, and DNA are directly or indirectly damaged. Meanwhile, chemotaxis and infiltration of neutrophile granulocytes and other inflammatory cells and production and secretion of inflammatory factors also play an important role in myocardial reperfusion injuries. These inflammatory responses not only directly damage myocardial tissues, but also immune vascular injuries are caused. Yet, the clinical application effect of preventing and treating myocardial reperfusion injuries by removing free oxygen (superoxide dismutase, reduced glutathione, etc.), improving the metabolism of ischemic tissues (e.g., creatine phosphate and trimetazidine), adding immune inhibitors and the like is not good. Therefore, an effective treatment method or medicament having a small side effect and used for prevention and treatment of myocardial ischemia reperfusion injuries is urgently needed.
A peroxide proliferator-activated receptor synergy promoter (PGC-1α) is a transcriptional co-activation factor and mediates a lot of energy metabolism related biological processes, especially in the aspect of the regulation of mitochondrial biosynthesis and oxidative metabolism conducted on various cells. In 2012, Boström found that PGC-1α expressions of skeletal muscles can be promoted through exercise, and while PGC-1α enables the level of fibronectin III-type domain containing proteins 5 (FNDC5) to rise, FNDC5 is a transmembrane protein with a total length of 196 amino acids of the fibronectin III-type domain containing proteins, and is a powerful inducer for inducing brown fat formation, the hydrolysis fragments thereof can be secreted into the blood to be circulated in the blood, and the FNDC5 content in myocardiums is very high, its functional effect on the heart is unclear at present, and clinical studies show that the FNDC5 expression in patients with heart failure is decreased somewhat. After an N-terminal signal peptide is removed from FNDC5, the FNDC5 cracks at the GLU142 position to form a polypeptide of about 110 amino acids, and the polypeptide is named irisin. At present, it is still unknown whether irisin has an effect on myocardial ischemia reperfusion injuries or not.